5. Visual evoked potentials, contrast sensitivity and foveal optical coherence tomography in Parkinson’s disease patients

Abstracts / Clinical Neurophysiology 127 (2016) e160–e164

Purpose: We propose that by covering central and temporal visual fields with either Z1 lenses plus side guards or elongated polarized lenses may suppress the PPR by altering the luminance and/or wavelength. Methods: 22 pediatric patients with Type 4 PPR (Waltz et al.) were tested with and without Z1 lenses using photic stimulation from 1 to 21 Hz. 19 patients had primary generalized epilepsy (5 JME & 14 Absence), 2 had reflex epilepsy and 2 had Dravet’s Syndrome. Results: Responses were classified into 3 groups: PPR disappearance, persistence or attenuation. 14 patients had reduced PPR (64%) and in 5 patients PPR disappeared (23%). 3 patients (13%) demonstrated persistence of the PPR with Z1 lenses. Several patients tested with side guards plus cobalt blue tint polarized lens sunglasses showed marked PPR reduction. Several patients tested with elongated polarized sunglasses covering the temporal visual field showed PPR attenuation. Placing a red lens over the photic stimulation lamp augmented the PPR from 1 to 19 Hz stimulation in several patients. A blue lens over the photic lamp resulted in attenuation or disappearance of the PPR at several photic stimulation frequencies in several patients. Conclusions: Z1 and other blue lenses reduced the PPR in nearly all patients. Possible mechanisms include polarization, reduction of luminance, and filtering of red light. Further testing of photosensitive patients will be performed. Comparisons will be made between Z1, elongated polarized, cobalt blue, red and green lenses. References Binnie CD, Jeavons PM. Photosensitive epilepsies. In: Roger J, Bureau M, Dravet C, et al., editors. Epileptic syndromes in infancy, childhood and adolescence. 2nd ed. London: John Libbey Eurotext; 1992. p. 299–305. Coppola et al. Suppressive efficacy by a commercially available blue lenson PPR in 610 photosensitive epilepsy patients. Epilepsia 2006;47(3):529–33. Jeavons PM, Harding GFA, editors. Photosensitive and epilepsy. Philadelphia: JB Lippincott; 1975. Kasteleijn-Nolst Trenit’e DGA, Hirsch E, Takahashi T. Photosensitivity, visual induced seizures and epileptic syndromes. In: Roger J, Bureau M, Dravet C, et al., editors. Epileptic syndromes in infancy, childhood and adolescence. 3rd ed. London: John Libbey; 2002. p. 369–85. Newmark ME, Penry JK, editors. Photosensitivity and epilepsy. New York: Raven Press; 1979. p. 128–9. Quirk JA, Fish DR, Smith SJM, et al. Incidence of photosensitive epilepsy: a prospective national study. Electroencephalogr Clin Neurophysiol 1995;95:260–7. Takahashi T, Tsukahara Y. Influence of colour on the photoconvulsive response. Electroencephalogr Clin Neurophysiol 1976;41:124–6. doi:10.1016/j.clinph.2015.10.054

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Design/methods: We retrospectively reviewed neuroimaging and EEG results of a consecutive cohort of 322 elders with new-onset epilepsy. The > 65 year-old patients were evaluated at the Centre Hospitalier Universitaire de Sherbrooke (CHUS) between January 2001 and October 2010. On imaging, TLA was assessed visually on axial images and graded on a 0–3 scale estimating sulcal widening and temporal horn ventricular enlargement. Measurement of the temporal horn radial width (THRW) was also acquired as a quantitative estimate of TLA. TLA was compared between subjects with epilepsy of unknown etiology (n = 127) and demented epileptic individuals of the same cohort (n = 10), as well as a healthy elderly control group (n = 31) and non-epileptic AD patients (n = 10). EEG interpretations were also analyzed, looking for correlation between temporal lobe atrophy and temporal epileptiform discharges, in the whole epileptic cohort. Results: MRI (46%) or CT (93%) was available for 112 patients with epilepsy of unknown etiology. Thirty-eight percent of elderly with new-onset epilepsy of unknown cause had significant temporal atrophy, using the dichotomized 0–3 scale (0–1 vs 2–3) or THRW. This was significantly more than the healthy control group (0%) after adjustment for age and sex (p = 0.000). As expected, individuals of the same cohort with epilepsy attributed to dementia had higher prevalence of significant TLA using both THRW and the visual scale (70.4%, p = 0.026 and 76.9% p = 0.021) as did patients with established AD (70% p = 0.040 and 60% p = 0.077). EEG results were available for 297 of the 322 patients (92.2%), including 125 of the 127 subjects with epilepsy of unknown etiology. Epileptiform discharges were present in 111/297 (37.3%) and 45/125 (36%) individuals respectively, of which 68.5% and 55.5% were found in temporal leads. No correlation was found between the presence of temporal lobe atrophy, using either dichotomized THRW or the visual scale, and temporal epileptiform activity (p = 0.312 and 0.469). Conclusions: A considerable proportion of elderly with new-onset epilepsy of unknown cause exhibit temporal lobe atrophy on brain imaging, which suggests that a degenerative disease such as AD could be underrecognized as a possible etiology. However, it appears there is no correlation between this atrophy and the temporal localization of epileptiform activity. Financial support: University Chair. doi:10.1016/j.clinph.2015.10.055

4. Temporal lobe atrophy: Frequent in elderly with epilepsy of unknown etiology—Emmanuelle Lapointe, Charles Deacon, Christian Bocti, Louis Royer-Perron, Stephen Cunnane, Alexandre Castellano (Université de Sherbrooke, Sherbrooke, Que, Canada)

5. Visual evoked potentials, contrast sensitivity and foveal optical coherence tomography in Parkinson’s disease patients—Shahnaz Miri a, Priyanka Chopra b, Sofya Glazman a, Lee Mylin a, Ivan Bodis-Wollner a,c (a Department of Neurology, SUNY Downstate Medical Center, United States , b School of Medicine, SUNY Downstate Medical Center, United States , c Department of Ophthalmology, SUNY Downstate Medical Center, United States)

Objective: To evaluate the degree of temporal lobe atrophy (TLA) in elderly patients with new-onset epilepsy, and its relation to temporal epileptiform discharges. Background: No etiology can be identified in as much as 30% to 50% of cases of new-onset epilepsy in the elderly, despite adequate investigation. Degenerative diseases, notably Alzheimer’s disease (AD), increase the risk of epilepsy, and are often underdiagnosed in routine clinical practice. Abnormal activity on electroencephalography (EEG) of demented epileptic individuals is most often found focally in temporal regions.

Background and objective: Impaired vision and remodeled foveal pit are demonstrated in Parkinson’s disease (PD) patients. Visual evoked potentials (VEPs) reflect abnormality anywhere in the retina to cortex pathways. We evaluated the correlation between the VEP, contrast sensitivity (CS) and foveal thickness in PD and assessed diagnostic yield of their combination. Methods: Ten PD (20 eyes) and eight HC subjects (16 eyes) were enrolled in the study. The two groups were matched for age, gender and ethnicity (P > 0.05). All subjects underwent standard neurological and ophthalmological examination to exclude any pathology. CS

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was evaluated using Pelli-Robson chart. Two-channel VEP was recorded on each subject with two different stimuli (pattern reversal, frequency of 2.3 cpd; and on/off pattern frequency of 4.6 cpd). N70 and P100 were recorded. Macular optical coherence tomography (OCT) scans were obtained using Zeiss-HD OCT and macular thickness, volume and ganglion cell layer-inner plexiform layer (GCL-IPL) thickness were extracted. Statistical analysis was performed using SPSS software (version 21.0). Results: PD patients had a significantly longer N70 (reversal pattern) and P100 (on/off pattern) latency (86.7 ± 10.2 and 132.9 ± 8.7 ms, respectively) compared to healthy controls (78.8 ± 6.6 and 125.5 ± 11.5 ms, respectively) (P = 0.01 and P = 0.03). CS score was significantly lower in PD patients (1.66 ± 0.21 vs. 1.89 ± 0.15; P = 0.001). PD patients had decreased thickness at the distance of 1.5–2.5 mm from the foveola (perifovea) (255.0 ± 6.5l vs. 264.9 ± 18.7l; P = 0.03). N70 latency was negatively correlated with CS (R = 0.419, P = 0.01) and average GCL-IPL thickness (R = 0.529, P = 0.001). CS was positively correlated with parafoveal thickness (R = 0.490, P = 0.002). A combination of parafoveal thickness and CS score yielded an AUC of 0.784, which increased to 0.844 when combined with N70 and P100 measures. Conclusion: Visual function is correlated with foveal morphology. A combination of VEP parameters, CS score, and foveal thickness has a high diagnostic yield for PD. doi:10.1016/j.clinph.2015.10.056

6. Frontopolar sharp potentials—Umang Modi, Paul Hwang (North York General Hospital, Toronto, Ont., Canada)

Sudden appearance of totally unexpected bisynchronous frontalpolar dominant unexpected potential initially embedded in eye blink with progressive recruitment and phase change. At times, it reaches up to 2.5 Hz, with awake background, and virtually minimal or limited spread to fronto-temporal or posterior frontal area on encephalogram. After very close examination and accepting wide variety of opinions, patient is being considered for epilepsy monitoring unit (EMU), so as same potential can be reproduced and evaluated for any fronto-polar epilepsies.

There are few unexpected potentials appears at fronto-polar region in EEG laboratory recording and must not escape, even though the patient has no additional oculographic leads. Potential described here, presented while ambulatory monitoring. The ocular potentials are mostly quite impressive and almost always give rise to marked eye movement artifacts in fronto-polar and anterior temporal leads. The use of polygraphic documentation makes the task much easier, as patient is being considered for EMU. When an REM phase occurs directly at sleep onset, the transition from drowsiness to REM is not very pronounced in the EEG, whereas the change from deep NREM sleep to REM is a very dramatic one (Matsuo, 1981). During photic stimulation, light from the flash stimulus may produce artifact in the fronto-polar leads (Fp1/Fp2). This artifact can be mistaken for photic driving due to the synchrony with the stimuli. The source maybe the retina (ERG) or from a nonphysiologic source such as a frontopolar electrode with high impedance creating a photo-cell. Covering the eye with a towel will block the input to the retina (ERG) and this should not be confused with the photoelectric effect (Tyner et al., 1983). The alpha rhythm may occasionally extend slightly into the superior frontal leads (F3, F4). Extension into the fronto-polar region (Fp1, Fp2) is practically unheard of. Apparent alpha rhythm in the fronto-polar leads may be very prominent in referential (unipolar) montages if the referential ear electrode picks up the posterior alpha rhythm. This is particularly com-mon when the mastoid region is used instead of the ear lobe (the mastoid being a preferred place with paste technique) (Niedermeyer’s Electroencephalography). Fronto-polar or orbito-frontal onset of seizures may be recorded from fronto-polar electrodes, and better resolved by supera-orbital or infra-orbital electrodes, sometimes it’s been referenced to midline electrodes like electrode on nose/chin, Fz, Cz or Pz. It is not uncommon for bilateral synchrony to occur in frontal lobe epilepsy (Atlas of EEG, 2013). Subtle lateralization may be present with bilateral synchronous activity, mainly during sleep. This lateralization could be misleading. Absence of any ictal or immediate post ictal slowing has been reported in patient with mesial frontal lobe epilepsy (Bautista et al., 1998). Behavioral manifestations with normal interictal EEG encountered in frontal lobe epilepsy may be misdiagnosed as psychogenic nonepileptic seizures. It emphasizes the need for early video-EEG